Fluorescent light-induced chromosome damage in human IMR-90 fibroblasts. Role of hydrogen peroxide and related free radicals.
Exposure of human fibroblasts (IMR-90) to cool-white fluorescent light causes chromatid breaks and exchanges. This chromatid damage is caused largely by the production of hydrogen peroxide (H2O2) since it can be prevented almost completely by the addition of catalase. In support of this conclusion, exogenous H2O2 is shown to induce chromatid breaks. The clastogenic amounts of H2O2 generated during light exposure are formed within the cell since cells illuminated in saline showed the same extent of damage as cells in culture medium. Addition of selenite to the cultures during light exposure significantly decreases the chromatid damage in a dose-related manner and may be necessary to maintain sufficient activity of glutathione peroxidase. The free hydroxyl radical, . OH, appears to be partially responsible for the light-induced chromatid damage. Of the free-radical scavengers tested, i.e., mannitol, vitamin E, and dimethyl sulfoxide, only mannitol, which scavenges . OH, significantly decreases the light-induced chromatid damage. Thus, both . OH and H2O2 formed within the cell during light exposure are agents that directly or indirectly cause chromatid damage.
D002374:Catalase / Q000502:physiology; D002460:Cell Line; D002842:Chromatids / Q000187:drug effects / Q000528:radiation effects; D002875:Chromosomes / Q000528:radiation effects*; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D005347:Fibroblasts; D005453:Fluorescence / Q000009:adverse effects*; D005609:Free Radicals; D006801:Humans; D006861:Hydrogen Peroxide / Q000096:biosynthesis / Q000494:pharmacology*; D008353:Mannitol / Q000494:pharmacology; D012643:Selenium / Q000494:pharmacology; D014810:Vitamin E / Q000494:pharmacology
D005609:Free Radicals; D014810:Vitamin E; D008353:Mannitol; D006861:Hydrogen Peroxide; D002374:Catalase; D012643:Selenium; D004121:Dimethyl Sulfoxide